5Centre for Neuroscience and Cell Biology, Department of Zoology, University of Coimbra, Coimbra, Portugal.

Corresponding author: Célia A. Aveleira, caveleira{at}ibili.uc.pt.

Abstract

OBJECTIVE Tumor necrosis factor-α (TNF-α) and interleukin-1 beta (IL-1β) are elevated in the vitreous of diabetic patients and in retinas
of diabetic rats associated with increased retinal vascular permeability. However, the molecular mechanisms underlying retinal
vascular permeability induced by these cytokines are poorly understood. In this study, the effects of IL-1β and TNF-α on retinal
endothelial cell permeability were compared and the molecular mechanisms by which TNF-α increases cell permeability were elucidated.

RESEARCH DESIGN AND METHODS Cytokine-induced retinal vascular permeability was measured in bovine retinal endothelial cells (BRECs) and rat retinas.
Western blotting, quantitative real-time PCR, and immunocytochemistry were performed to determine tight junction protein expression
and localization.

CONCLUSIONS These results suggest that PKCζ may provide a specific therapeutic target for the prevention of vascular permeability in
retinal diseases characterized by elevated TNF-α, including diabetic retinopathy.

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